Study Objectives: To determine prevalence and heritability of insomnia during middle/late childhood and adolescence; examine longitudinal associations in insomnia over time; and assess the extent to which genetic and environmental factors on insomnia remain stable, or whether new factors come into play, across this developmental period.Design: Longitudinal twin study.Setting: Academic medical center.Patients or Participants: There were 739 complete monozygotic twin pairs (52%) and 672 complete dizygotic twin pairs (48%) initially enrolled and were followed up at three additional time points (waves). Mode ages at each wave were 8, 10, 14, and 15 y (ages ranged from 8-18 y).Interventions: None.Measurements and Results: Clinical ratings of insomnia symptoms were assessed using the Child and Adolescent Psychiatric Assessment (CAPA) by trained clinicians, and rated according to Diagnostic and Statistical Manual of Mental Disorders, 3rd Edition-Revised criteria for presence of "clinically significant insomnia," over four sequential waves. Insomnia symptoms were prevalent but significantly decreased across the four waves (ranging from 16.6% to 31.2%). "Clinically significant insomnia" was moderately heritable at all waves (h2 range = 14% to 38%), and the remaining source of variance was the nonshared environment. Multivariate models indicated that genetic influences at wave 1 contributed to insomnia at all subsequent waves, and that new genetic influences came into play at wave 2, which further contributed to stability of symptoms. Nonshared environmental influences were time-specific.Conclusion: Insomnia is prevalent in childhood and adolescence, and is moderately heritable. The progression of insomnia across this developmental time period is influenced by stable as well as new genetic factors that come into play at wave 2 (modal age 10 y). Molecular genetic studies should now identify genes related to insomnia progression during childhood and adolescence.

Alcohol consumption is differentially associated with social and health harms across U.S. ethnic groups. Native Americans, Hispanics, and Blacks are disadvantaged by alcohol-attributed harms compared with Whites and Asians. Ethnicities with higher rates of risky drinking experience higher rates of drinking harms. Other factors that could contribute to the different effects of alcohol by ethnicity are social disadvantage, acculturation, drink preferences, and alcohol metabolism. This article examines the relationship of ethnicity and drinking to (1) unintentional injuries, (2) intentional injuries, (3) fetal alcohol syndrome (FAS), (4) gastrointestinal diseases, (5) cardiovascular diseases, (6) cancers, (7) diabetes, and (8) infectious diseases. Reviewed evidence shows that Native Americans have a disproportionate risk for alcohol-related motor vehicle fatalities, suicides and violence, FAS, and liver disease mortality. Hispanics are at increased risk for alcohol-related motor vehicle fatalities, suicide, liver disease, and cirrhosis mortality; and Blacks have increased risk for alcohol-related relationship violence, FAS, heart disease, and some cancers. However, the scientific evidence is incomplete for each of these harms. More research is needed on the relationship of alcohol consumption to cancers, diabetes, and HIV/AIDS across ethnic groups. Studies also are needed to delineate the mechanisms that give rise to and sustain these disparities in order to inform prevention strategies.